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How long would you like to live? Three score years and ten, as the Bible suggests? Long enough to see your great-grandchildren graduate from college or get married? Longer? Forever? Or maybe you would settle for living as long as humanly possible—a span which might depend on how young you are now, and hence how likely you are to reap the benefits of longevity breakthroughs to come.

Before you answer, you also need to consider what you are willing to do for those extra years. Are you willing to religiously eat right—however nutritionists currently define “right”—or even semi-starve yourself? Exercise, either moderately or intensely, depending on the wisdom of the day? Are you prepared to take resveratrol or coenzyme Q10? Add the proper dose of green tea to your diet? Would you give up coffee? You name it, someone has probably suggested it over the years as a means of delaying death.

And since the newest research suggests that extreme longevity is determined largely by genes, you might also want to know, as I do, whose genes you’ve inherited (my father died at 93, my mother at 71) and which aspects of lifestyle, diet, and the environment influence those genes most. Researchers have been busier than ever lately decoding the genes of longevity, all in hopes of bottling the formula for those less well-endowed.


It’s not easy figuring out how to maximize your years on this planet.

Until the 1990s, questions of how we age, how long we’ll last, and what we can do about it were mostly the purview of quacks, philosophers, and the odd evolutionary biologist speculating on why different animals age at vastly different rates. Medical researchers were not all that interested. Aging, after all, is not a disease but a natural process, the accumulation of defects that our bodies simply do not have the wherewithal to repair. And medicine was traditionally taught, studied, and practiced in disciplines, divided up by organ, body part, and disease. As a result, neither researchers nor physicians nor the government agencies that fund medical research saw fit to study aging itself. In the early 1990s, when Nir Barzilai, now the director of the Institute for Aging Research at Albert Einstein College of Medicine in New York City, decided to study aging, he did so in part because the competition was so sparse. “Why compete with 100,000 people studying cancer,” he asks, “when maybe 10 people were doing aging research?”

The past two decades have changed all that. Researchers have taken to studying long-lived versions of everything from yeast and nematode worms to rats, mice, monkeys, and (of course) humans, hoping to identify the biological mechanisms that determine longevity and that perhaps show how to extend it. They have created worms that live 10 times longer than normal and fruit flies that live up to four times as long. Most recently, they have taken mice in late middle age and lengthened the remainder of their lives by an average of 30 to 40 percent with a drug called rapamycin, an antifungal agent also used to suppress immune responses in transplant patients.

David Sharp, chairman of the department of molecular medicine at the University of Texas Health Science Center, noticed the benefits of the agent and wondered whether it might be used to lengthen human life, too. That is an open question for a drug that works in mice. (It’s relatively easy to cure cancer in laboratory mice—“If you can’t cure cancer in a mouse,” a cancer researcher once said to me, “then you should change careers”—but certainly not easy in people. Maybe the same goes for life extension.) The National Institutes of Aging gave Sharp’s institute a $5 million grant to see if it could find answers. “We have this institute in a research park in Texas,” Sharp says. “We joke that it’s become Rapaland, because everybody is looking at various aspects of rapamycin.”

With each newly discovered long-lived organism or potential “longevity drug,” a growing list of researchers have proffered theories and embarked on projects to unravel the mechanism. The surging interest and associated funding have been fueled by recognition of aging as the catchall risk factor for the diseases that eventually kill us all. Aging increases exponentially our risk of getting heart disease, cancer, and diabetes. Our likelihood of dying from any of these diseases is vanishingly small in our early twenties but doubles every eight to nine years. By middle age it begins to get significant, and we start to see friends and former classmates falling by the wayside. Then it relentlessly doubles and doubles again until we succumb ourselves. When researchers study centenarians, people who live to be 100 or older—as Barzilai and his colleagues have been doing at Albert Einstein for more than a decade—they find that these well-aged individuals are certainly not immune to chronic diseases, but they get them later in life. If they get cancer, it does not kill them or it progresses very slowly.

“Aging is an underlying timing mechanism for all chronic diseases,” says David Harrison, a collaborator with Sharp and other rapamycin researchers at the Jackson Laboratory in Maine. The hope is that by slowing the aging processes, the chronic diseases associated with aging will be delayed or prevented along the way. “If we can retard aging a little bit,” Harrison says, “we can actually improve health not just from one disease but from cancer, atherosclerosis, diabetes, osteoporosis, arthritis, Alzheimer’s, Parkinson’s—from most of the bad things. We get an increase in healthy life span.”

Researchers like Harrison and Sharp are not hoping to stop the aging process entirely (although some visionaries, like Aubrey de Grey and Raymond Kurzweil, certainly are). They are not even thinking about extending the human life span to 150 or 200 years, at least not in the short term. Their stated intent is to find whatever modest extensions in life span nature has to offer—maybe adding 10 or 15 years to the average healthy life—and, more important, keeping us healthier as we age.